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hypotension/protease
Linkki tallennetaan leikepöydälle
Sivu 1 alkaen 103 tuloksia
Suppression of peripheral sympathetic activity underlies protease-activated receptor 2-mediated hypotension.
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Protease-activated receptor (PAR)-2 is expressed in endothelial cells and vascular smooth muscle cells. It plays a crucial role in regulating blood pressure via the modulation of peripheral vascular tone. Although some reports have suggested involvement of a neurogenic mechanism in PAR-2-induced
Protease-activated receptor-2 involvement in hypotension in normal and endotoxemic rats in vivo.
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BACKGROUND
The protease-activated receptor-2 (PAR-2) is expressed by vascular endothelial cells and upregulated by lipopolysaccharide (LPS) in vitro. PAR-2 is activated by a tethered ligand created after proteolytic cleavage by trypsin or experimentally by a synthetic agonist peptide (PAR-2AP)
Activated protein C prevents endotoxin-induced hypotension in rats by inhibiting excessive production of nitric oxide.
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BACKGROUND
Excessive production of nitric oxide (NO) by the inducible isoform of NO synthase (iNOS) is critically involved in endotoxin (ET)-induced hypotension. Tumor necrosis factor-alpha (TNF-alpha) plays an important role in induction of iNOS. Because activated protein C (APC), a physiological
Hypotension and inflammatory cytokine gene expression triggered by factor Xa-nitric oxide signaling.
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The signaling pathway initiated by factor Xa on vascular endothelial cells was investigated. Factor Xa stimulated a 5- to 10-fold increased release of nitric oxide (NO) in a dose-dependent reaction (0.1-2.5 microG/ml) unaffected by the thrombin inhibitor hirudin but abolished by active site
Pancreatic protease inhibition during shock attenuates cell activation and peripheral inflammation.
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Intestinal ischemia contributes to shock-induced multiple organ failure. Our recent evidence suggests that pancreatic proteases may be involved in the formation of inflammatory activators within an ischemic intestine. These inflammatory mediators are released early into the circulation and may
Acute blood pressure effects of selected serine proteases in normotensive rats and dogs.
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The effects of bolus intravenous injections of various serine proteases (thrombin, trypsin, plasmin, neutrophil elastase and chymotrypsin) on arterial blood pressure were evaluated in anesthetized, normotensive rats. The activity to intravenous trypsin was also studied in anesthetized, normotensive
Cardiovascular responses mediated by protease-activated receptor-2 (PAR-2) and thrombin receptor (PAR-1) are distinguished in mice deficient in PAR-2 or PAR-1.
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We developed mice deficient in protease-activated receptor-2 (PAR-2) or PAR-1 to explore the pathophysiological functions of these receptors. In this report, we evaluated mean arterial pressure and heart rate (HR) changes in response to PAR-1 or PAR-2 activation in anesthetized wild-type (WT),
Effect of a new synthetic protease inhibitor on beta-endorphin release during acute pancreatitis in dogs.
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The effect on endogenous beta-endorphins of a new synthetic protease inhibitor was studied in acute pancreatitis. Pancreatitis was induced by the injection of autologous bile mixed with trypsin into the main pancreatic duct after ligation of the accessory duct. Plasma beta-endorphin concentrations
The effects of the protease inhibitor, aprotinin, on the course of shock induced by endotoxin in cats.
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The administration of endotoxin derived from Escherichia coli to anaesthetized cats resulted, within the first 5 min, in an initial increase in right atrial pressure and a reduction in systemic arterial blood pressure. Over the next 2 h shock was characterized by a reduced cardiac output,
Effect of the protease inhibitor aprotinin on renal hemodynamics in the pig.
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Aprotinin, the serine protease inhibitor that also inhibits glandular (urinary) kallikrein, or vehicle was infused into the aorta above the renal arteries of anesthetized pigs. Renal hemodynamic and functional parameters were followed over time and during hemorrhagic hypotension. Both renal cortical
Protease-activated receptor 2 activation inhibits N-type Ca2+ currents in rat peripheral sympathetic neurons.
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The protease-activated receptor (PAR)-2 is highly expressed in endothelial cells and vascular smooth muscle cells. It plays a crucial role in regulating blood pressure via the modulation of peripheral vascular tone. Although several mechanisms have been suggested to explain PAR-2-induced
Cystatin C, a protease inhibitor, in degenerating rat hippocampal neurons following transient forebrain ischemia.
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Cystatin C, a cysteine protease inhibitor produced by the choroid plexus and found in CSF at high concentrations, may have an important role in brain injury. We used the two-vessel occlusion model with hypotension to induce transient forebrain ischemia (TFI) in rats for 10 min and then examined
Involvement of EDHF in the hypotension and increased gastric mucosal blood flow caused by PAR-2 activation in rats.
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1. Agonists for protease-activated receptor-2 (PAR-2) cause hypotension and an increase in gastric mucosal blood flow (GMBF) in vivo. We thus studied the mechanisms underlying the circulatory modulation by PAR-2 activation in vivo, especially with respect to involvement of endothelium-derived
Pancreatic proteases and intestinal mucosal injury after ischemia and reperfusion in the pig.
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Intraluminal pancreatic proteases have been proposed to play a pathogenic role in the injury seen after ischemia and reperfusion of the small intestinal mucosa. Intestinal ischemia can be detected by indirect intramucosal pH measurements using tonometry. In this study, pigs were subjected to
Beneficial effects of LEX032, a novel recombinant serine protease inhibitor, in murine traumatic shock.
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The effects of LEX032, a novel recombinant serine protease inhibitor (i.e., serpin), were investigated in an experimental model of Noble-Collip drum shock. Pentobarbital-anesthetized rats subjected to drum trauma and receiving only the vehicle, developed severe traumatic shock with hypotension.
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